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Cessation of drug use in chronic opiate abusers produces a severe withdrawal syndrome that is highly aversive, and avoidance of withdrawal or associated stimuli is a major factor contributing to opiate abuse. Increased noradrenaline in the brain has long been implicated in opiate withdrawal, but it has not been clear which noradrenergic systems are(More)
The nucleus accumbens (NAcc) can be subdivided into 'core' and 'shell' based on anatomical connections and histochemical markers. Previous studies have demonstrated dopamine-beta-hydroxylase immunoreactive (DBH-ir) fibers in the NAcc shell, but the source of these noradrenergic (NE) afferents has not been determined. Therefore, we have investigated in(More)
Hyperactivity of brain norepinephrine (NE) systems has long been implicated in mechanisms of opiate withdrawal (OW). However, little is known about where elevated NE may act to promote OW. Here we report that the bed nucleus of the stria terminalis (BNST), the densest NE target in the brain, is critical for NE actions in OW. (1) Many BNST neurons become(More)
Microinjection of amphetamine into the ventrolateral region of the striatum results in compulsive and intense oral stereotypies in the rat. Although these stereotyped behaviors are known to be a direct result of excessive stimulation of the striatal dopamine neurons, the relative roles of the D1 and D2 receptors in oral stereotypies are not clearly(More)
Lesions of the subthalamic nucleus block behavioral effects of nigrostriatal dopamine depletion in rats and primates, but the contribution of this region to the molecular effects of dopaminergic lesions is unknown. The effects of subthalamic nucleus lesions alone or in combination with a 6-hydroxydopamine-induced lesion of the substantia nigra were examined(More)
In the conditioned reinforcement paradigm, animals learn a new instrumental response reinforced solely by conditioned reward (a stimulus that has previously been associated with primary reward). It has been shown that psychostimulants potentiate responding for conditioned reward and there is evidence that the nucleus accumbens is involved in this effect.(More)
Cocaine is believed to exert its psychostimulant effects through activation of the mesocorticolimbic system. Although the nucleus accumbens, in particular, has been hypothesized as the site of action of cocaine's stimulating effects, there is no direct evidence that microinjection of cocaine into this region produces behavioral activation. The present(More)
Cholinomimetic drugs are known to induce changes in perioral behavior in rodents, characterized primarily by “purposeless” chewing mevements, but little is known about their central sites of action. Using observational methods, the effects of direct microinfusion of a mixture of physostigmine and acetylcholine (PS/Ach, 0, 0.5, 2.5, 5.0 μg of each in 0.5 μl(More)
A model of basal ganglia functioning proposed a few years ago suggests that increased and decreased activity in basal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic movements as seen in Huntington's disease or after treatment with L-dopa and neuroleptics, respectively. Although the basic features of this(More)
It has been shown that infusion of certain neuropeptides into the ventral tegmental area (VTA) results in increased motor activity and enhanced dopamine turnover in the nucleus accumbens. In the present experiments, substance P (SP), neurotensin (NT), d-ala-metenkephalin (DALA) and morphine sulfate (MS) were injected bilaterally into the VTA and their(More)